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Differential Expression and Modulation of Costimulatory Molecules CD80 and CD86 on Monocytes from Patients with Systemic Lupus Erythematosus
Author(s) -
LIU M.F.,
LI J.S.,
WENG T.H.,
LEI H.Y.
Publication year - 1999
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1046/j.1365-3083.1999.00452.x
Subject(s) - cd80 , cd86 , immunology , medicine , immune system , biology , cd40 , genetics , t cell , in vitro , cytotoxic t cell
Patients with systemic lupus erythematosus (SLE) were recently shown to be defective in costimulatory molecule CD80 (B7‐1) expression on antigen‐presenting cells. This study was undertaken to further investigate the expression and cytokine regulation of both CD80 and CD86 (B7‐2) on monocytes from patients with SLE. Freshly isolated and in vitro cytokine‐stimulated peripheral blood mononuclear cells from 13 patients with SLE and 10 healthy subjects were analysed, cytometrically with dual‐fluorescence staining, to detect expression of CD80 and CD86 in the CD14 + monocyte population. The results showed that, as in normal individuals, an overwhelming majority (95.62 ± 3.54%) of monocytes from patients with SLE expressed the CD86 molecule, but only a few monocytes (5.54 ± 4.36%) had detectable CD80 expression. The effects of interleukin‐10 (IL‐10) on the expression of CD80 and CD86 on monocytes from patients with SLE and normal controls were similar. IL‐10 down‐regulated the expression of CD86 while it slightly enhanced that of CD80. Interferon‐γ (IFN‐γ) increased both CD80 and CD86 expression on monocytes from both SLE patients and normal groups, albeit less significantly in the former than in the latter, i.e. CD80: 142.84 ± 65.99% versus 226.08 ± 78.90%, P < 0.05; and CD86: 72.55 ± 74.23% versus 153.99 ± 94.14%, P < 0.05, when expressed as percentage modulation. Granulocyte–macrophage colony‐stimulating factor (GM‐CSF) showed a capacity for up‐regulation of CD80 and CD86 expression on monocytes, of a magnitude that was similar both in patients with SLE and in normal subjects. We concluded that CD80 and CD86 were differentially expressed and modulated on monocytes and the defective IFN‐γ‐induced up‐regulation of CD80 and CD86 expression on SLE monocytes might be a factor in the pathogenesis of SLE.